Drug Interactions Newsletter Archives
Released Issues
2011; Volume 3
Issue 46: Question: How can the coadministration of carbamazepine (Carbatrol; Equetro; Tegretol) increase the clearance of quetiapine (Seroquel) by 7-fold?
Issue 44: Question: How does ibuprofen (Advil; Motrin) inhibit the antithrombotic activity of aspirin?
Issue 38: Question: How does the use of nitrates (nitroglycerin) in patients taking type 5 phosphodiesterase (PDE5) inhibitors, sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra) lower the blood pressure?
Issue 30: Question: How does the use of ketoconazole increase the patient's drug exposure of the antipsychotic, quetiapine (Seroquel) by over 522%?
Issue 26: Question: What are some common medications known to inhibit the activity of thiopurine methyltransferase (TPMT)?
Issue 22: Question: Why should the proton pump inhibitor omeprazole (Prilosec) be avoided in treatment-experienced HIV infected patients taking the protease inhibitor, atazanavir (Reyataz)?
Issue 18: Question: Why should fluoxetine (Prozac) not be given to patients with breast cancer that is being treated with tamoxifen (Nolvadex)?
Issue 14: Question: How does the combination of itraconazole (Sporanox) and gemfibrozil (Lopid) cause a 19-fold increase in repaglinide (Prandin) plasma concentrations?
Issue 10: Question: How does disulfiram (Antabuse) interact with alcohol (ethanol) to cause patients to get so sick?
Issue 6: Question: Which loop diuretic has the potential to interact with azathioprine (Imuran; Azasan) due to the inhibition of thiopurine methyltransferase (TPMT)?
Issue 2: Question: What type of inhibition does gemfibrozil confer onto CYP2C8 and what medications could be affected?
2010; Volume 2
Issue 46: Question: Can the use of proton pump inhibitors (PPI) decrease the absorption (or bioavailability) of oral iron replacement in patients with iron deficiency anemia?
Issue 42: Question: How long after stopping St. John's wort (Hypericum perforatum) does the inductive effects on cytochrome P450 (CYP) 3A4 enzymes continue to last?
Issue 38: Question: Why should the protease inhibitor, atazanavir (Reyataz), be used with caution in combination with the histamine-2 (H2) receptor antagonist, ranitidine (Zantac)?
Issue 34: Question: What is the mechanism by which tamoxifen's (Nolvadex) efficacy in treating breast cancer is decreased by the use of paroxetine (Paxil)?
Issue 30: Question: Does metronidazole (Flagyl) use with lopinavir/ritonavir oral solution (Kaletra) cause a disulfiram like reaction and is this risk clinically relevant?
Issue 26: Question: What is the mechanism of action by which gemfibrozil (Lopid) increases the blood levels of repaglinide (Prandin) 8-fold?
Issue 22: Question: What does it mean for a drug to be a mechanism-based inhibitor of cytochrome P-450 (CYP) 3A4?
Issue 18: Question: How does aluminum hydroxide chelate with and reduce the intestinal absorption of the fluoroquinolone antibiotic, levofloxacin (Levaquin)?
Issue 14: Question: What is the only non-nucleoside reverse transcriptase inhibitor (NNRTI) used in the treatment of HIV infection that is known to be an inhibitor of cytochrome P450 (CYP) 3A4?
Issue 10: Question: Is there any evidence that has determined the impact histamine-2 receptor antagonists (H2RA) have on oral iron replacement therapy?
Issue 6: Question: What medications are known substrates for UDP-glucuronosyltransferase (UGT) 1A1 enzyme mediated drug interactions?
Issue 2: Question: Does Pharmacology Weekly have a drug reference tool to help clinicians with managing HIV patients, especially since the medications they are on are known to cause significant drug interactions?
2009; Volume 1
Issue 48: Question: Why is it so important to consider several dosage reductions in a patient on stable doses of the oral anticoagulant, warfarin (Coumadin, Jantoven), when initiating amiodarone (Cordarone, Pacerone)?
Issue 47: Question: What is a [I]/Ki ratio and how can a clinician use it to predict the likelihood for a drug-drug interaction?
Issue 46: Question: What is an inhibitory constant (Ki) and how does it relate to understanding drug interactions?
Issue 45: Question: Are there any updates to the drug interaction between clopidogrel (Plavix) and proton pump inhibitors in patients who have received percutaneous coronary intervention (PCI) involving stent placement?
Issue 44: Question: What is the mechanism by which histamine-2 receptor antagonists (H2RA) decrease the absorption (or bioavailability) of oral iron replacement in patients with iron deficiency anemia?
Issue 43: Question: What are some common medications classified as weak, moderate and strong inhibitors of CYP3A4?
Issue 42: Question: What medications are substrates for UDP-glucuronosyltransferase (UGT) 2B7 enzyme mediated drug interactions?
Issue 41: Question: What effect does the antibiotic clarithromycin (Biaxin®) have on the cytochrome P450 (CYP) 3A4 enzyme?
Issue 40: Question: Why is the HMG CoA reductase inhibitor (statin), specifically fluvastatin (Lescol®; Lescol XL®) considered to be safer in combination with cyclosporine (Gengraf®; Neoral®; Sandimmune®) compared to other statins in the treatment of hyperlipidemia?
Issue 39: Question: What is the process to determine if medications are to be classified as weak, moderate or strong inhibitors of CYP3A4?
Issue 38: Question: What is the mechanism by which naproxen (Aleve®; Anaprox®; Anaprox DS®; Naprosyn®) can increase the serum concentrations of methotrexate (Rheumatrex®; Trexall®) and risk for significant side effects such as bone marrow suppression or hepatotoxicity?
Issue 37: Question: Why is lovastatin (Mevacor®) absolutely contraindicated in human immunodeficiency virus (HIV) infected patients taking protease inhibitor (PI) based highly active antiretroviral therapy (HAART)?
Issue 36: Question: Which of the eleven UDP-glucuronosyltransferase (UGT) enzymes are most likely to be involved in drug metabolism and thus targets for drug interactions?
Issue 35: Question: What factors are known to influence the biologic response to drug therapy that all healthcare providers should take into consideration?
Issue 34: Question: What medications commonly used in clinical practice rely upon the cell surface efflux transporter breast cancer resistance protein (BCRP) and are subject to drug interactions?
Issue 33: Question: What is the specific mechanism by which aluminum hydroxide inhibits the absorption of levothyroxine (T4; Levothroid®, Levoxyl®, Synthroid®, and Unithroid®)?
Issue 32: Question: What is the mechanism by which the cholesterol absorption inhibitor, ezetimibe (Zetia®), increases the blood concentrations of cyclosporine (Gengraf®, Sandimmune®, Neoral®) and is it clinically relevant?
Issue 31: Question: Why should the xanthine oxidase inhibitor, febuxostat (Uloric®) not be given to patients taking the immunosuppressant azathioprine (Azasan®, Imuran®)?
Issue 30: Question: What drug characteristics predispose it to be significantly elevated in the body in the presence of an inhibitor of metabolism?
Issue 29: Question: Why is eplerenone (Inspra®) prone to more drug interactions than spironolactone (Aldactone®)?
Issue 28: Question: Are there any studies evaluating the use of histamine-2 receptor antagonists (H2RA) with clopidogrel (Plavix®) as it relates to clopidogrel's ability to prevent stent thrombosis or platelet aggregation?
Issue 27: Question: Are there any known drug interactions between histamine-2 receptor antagonists (H2RA) and clopidogrel (Plavix®) that could compromise the efficacy on platelet inhibition?
Issue 26: Question: What data are available regarding the efficacy of clopidogrel (Plavix®) on platelet inhibition or reactivity when given with a proton pump inhibitor (PPI)?
Issue 25: Question: What studies are available related to the drug interaction between proton pump inhibitors (PPI) and clopidogrel (Plavix®) on cardiovascular (CV) related endpoints or outcomes?
Issue 24: Question: Are there any differences among the proton pump inhibitors (PPI) in their ability to inhibit the activation of clopidogrel (Plavix®) through the cytochrome P450 (CYP) enzyme system?
Issue 23: Question: What is the mechanism by which metronidazole (Flagyl®) causes clinically relevant increases in warfarin (Coumadin®, Jantoven®) blood concentrations and puts the patient at risk for bleeding?
Issue 22: Question: What is the mechanism by which the immunosuppressant, cyclosporine (Gengraf®, Sandimmune®, Neoral®) increases the cholesterol absorption inhibitor, ezetimibe (Zetia®), blood concentrations over 3-fold?
Issue 21: Question: Which one of the fibric acid derivatives (gemfibrozil or fenofibrate) is known to cause drug interactions through inhibition of the glucuronidation via UDP-glucuronosyltransferase (UGT)?
Issue 20: Question: What are the common efflux transporters involved in drug transport and drug-drug interactions?
Issue 19: Question: What are the common influx transporters involved in drug transport and drug-drug interactions?
Issue 18: Question: How do calcium supplements (such as calcium carbonate) significantly reduce the absorption or bioavailability of ciprofloxacin (Cipro®) thereby increasing the risk of therapeutic failure?
Issue 17: Question: Part 2: What is the average dose reduction of digoxin (Digitek®; Lanoxin®) needed when used in combination with the antiarrhythmic medication, amiodarone (Cordarone®)?
Issue 16: Question: Part 1: What is the mechanism by which digoxin (Digitek®; Lanoxin®) concentrations are significantly increased with the use of amiodarone (Cordarone®)?
Issue 15: Question: How does the protease inhibitor, atazanavir (Reyataz®) that is used in the treatment of human immunodeficiency virus (HIV) significantly increase the levels of the statin, rosuvastatin (Crestor®) if they have different CYP450 profiles?
Issue 14: Question: What is the mechanism by which the proton pump inhibitor, omeprazole (Prilosec®), reduces the antiplatelet effects of clopidogrel (Plavix®) thereby decreasing its cardioprotective effects?
Issue 13: Question: If not primarily by decreasing renal filtration, then by what mechanism does the NSAID ibuprofen (Advil®; Motrin®) increase methotrexate (Rheumatrex®; Trexall®) concentrations thereby increasing the patient's risk for myelosuppression and hepatotoxicity?
Issue 12: Question: How does the interaction between allopurinol (Zyloprim®, Aloprim®) and the immunosuppressant, azathioprine (Imuran®; Azasan®) increase the risk of significant reductions in WBCs?
Issue 11: Question: What are the various mechanisms for drug interactions that all clinicians need to know?
Issue 10: Question: Part 2: How common is it for patients taking tramadol (Ultram®; Ultram ER®; Ultracet™) and SSRI antidepressants to develop serotonin syndrome?
Issue 9: Question: Part 1: How does the opioid analgesic tramadol (Ultram®; Ultram ER®, Ultracet®) increase the risk for developing serotonin syndrome in patients taking SSRI antidepressant medications?
Issue 8: Question: How does coadministration of the antidepressant paroxetine (Paxil®; Paxil CR®) with atomoxetine (Strattera®) cause a 6 to 8 fold increase in atomoxetine concentrations and is this increase clinically meaningful?
Issue 7: Question: How does cyclosporine (Gengraf®; Sandimmune®; Neoral®) cause a 5-12 fold increase in pravastatin (Pravachol®) concentrations even though pravastatin is not a substrate of the CYP450 enzyme system?
Issue 6: Question: How can the use of proton pump inhibitors (i.e., omeprazole, lansoprazole) significantly decrease the absorption of itraconazole (Sporanox) thereby increasing the risk of antifungal treatment failure?
Issue 5: Question: How does trimethoprim/sulfamethoxazole (Bactrim™;Bactrim™DS; Septra® DS) result in clinically significant increases in the INR in patients on stable doses of warfarin (Coumadin®; Jantoven®) and thereby put them at significant risk for bleeding?
Issue 4: Question: Why is simvastatin (Zocor) contraindicated in HIV patients on protease inhibitors (PIs) but not those on non-nucleoside reverse transcriptase inhibitors (NNRTIs)?
Issue 3: Question: Why should patients taking nitrates (nitroglycerin injection, tabs, patches or ointments) for their heart disease not receive type 5 phosphodiesterase inhibitors (Viagra, Cialis, or Levitra) for the treatment of erectile dysfunction (ED)?
Issue 2: Question: How does valproate (Depakene® or Depakote®) interact with lamotrigine (Lamictal®) to increase the risk of potentially life threatening skin rashes, such as Steven-Johnson Syndrome, when neither one of the drugs are known to be significant substrates or inhibitors of the CYP450 enzyme system?
Issue 1: Question: Why is there a need to understand drug interactions? Can we not explain them by only looking at the CYP450 system?
Share
